Effect of salivary exosomal miR-25-3p on periodontitis with insulin resistance
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA781584 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR16975319.fastq.gz | Fastqsanger.gz | |||
| SRR16975320.fastq.gz | Fastqsanger.gz | |||
| SRR16975321.fastq.gz | Fastqsanger.gz | |||
| SRR16975322.fastq.gz | Fastqsanger.gz |
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Project description:Salivary exsomal miRNAs may play important role in the pathogenesis of chronic inflammatory disease, such as periodontitis. There are many studies which suggested the connection between periodontitis and systemic disease, however, the role of specific miRNA as a intersection of periontitis and diabetes are not elucidated. We suggested miR-25-3p as possible common mediator in the pathogenesis of periodontitis and diabetes.
2021-11-20 | GSE189107 | GEO
Project description:Periodontitis is caused by an oral microbial dysbiosis-mediated imbalance of the local immune microenvironment, which is promoted by insulin resistance and obesity. The prevalence and severity of periodontitis is higher in patients with type 2 diabetes than in healthy individuals, possibly because of differences in immune responses. The level of glycemic control also affects the saliva profile, which may further promote periodontal disease in diabetes patients. Therefore, we compared the salivary exosomal miRNA profiles of patients with type 2 diabetes with those of healthy individuals, and we found that exosomal miR-25-3p in saliva is significantly enriched (by approximately 2-fold, p < 0.01) in obese patients with type 2 diabetes. We also identified CD69 mRNA as a miR-25-3p target that regulates both activation of γδ T cells and the inflammatory response. Knockdown of CD69 increased (by approximately 2-fold) interleukin-17A production of γδ T cells in vitro. To evaluate the role of exosomal miRNA on progression of periodontitis, we analyzed regional immune cells in both periodontal tissues and lymph nodes from mice with periodontitis. We found that diet-induced obesity increased the population of infiltrating pro-inflammatory immune cells in the gingiva and regional lymph nodes of these mice. Treatment with miR-25-3p inhibitors prevented the local in vivo inflammatory response in mice with periodontitis and diet-induced obesity. Finally, we showed that suppression of interleukin 17-mediated local inflammation by a miR-25-3p inhibitor alleviated (by approximately 34%) ligature-induced periodontal alveolar bone loss in mice. Taken together, these data suggest that exosomal miR-25-3p in saliva contributes to development and progression of diabetes-associated periodontitis. Discovery of additional miR-25-3p targets may provide critical insights into developing drugs to treat periodontitis by regulating γδ T cell-mediated local inflammation.
| S-EPMC8777127 | biostudies-literature
Project description:We report the application of high throughput Illumina sequencing for profiling of small RNAs in saliva of patients who were diagnosed with chronic periodontitis as compared to healthy controls. To date, there is no published literature on salivary microRNA profiling done using the high throughput next-generation sequencing analysis in patients diagnosed with chronic periodontitis. Also, this is the first study of its kind done in an Indian population. The objectives of the study were to profile microRNAs expressed in saliva of patients diagnosed with chronic periodontitis, to identify differentially expressed microRNAs between chronic periodontitis and healthy patients and to identify putative salivary microRNAs which can serve as biomarkers for periodontal disease.
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Project description:To elucidate whether exosomal hsa-miR199a-3p plays a role in neuroblastoma tumorigenesis, a miRNA-seq analysis on plasma exosomal miRNA from neuroblastoma patients and normal controls.
2019-03-08 | GSE128004 | GEO
Project description:Exosomes which are nano-vesicles and released from living cells, have attracted more attention as an important mediator for cell-to-cell communication. Given that obesity often causes insulin resistance, it is significant to test whether exosomes derived from obesity adipose tissue possess any capacity in regulating insulin sensitivity. In this study we purified exosomes from the adipose tissue. Exosomes derived from ob/ob mice (Ob-exosomes) and B6 mice fed a high-fat diet (HFD-exosomes) displayed similar size and molecular maker to those originated from the normal B6 mice (WT-exosomes), but their regulatory role in insulin sensitivity was opposite. Abundant exosomal miRNAs were detected by the Next Generation Sequencing. Ob-exosomes encapsulated the lower levels of miR-141-3p compared to WT-exosomes, furthermore, miR-141-3p can be effectively delivered into AML12 cells accompanied by the absorption of Ob-exosomes and WT-exosomes. But the absorption of miR-141-3p from adipose tissues to AML12 cells could be blocked by GW4869, an inhibitor of exosome biogenesis and release. Importantly, the exosomal miR-141-3p functionally down-regulated its target gene Pten expression in AML12 cells, and the knockdown of miR-141-3p inhibited the insulin response and glucose uptake in AML12 cells, however Ob-exosomes-mediated inhibitory effects on insulin function disappeared after overexpression of miR-141-3p. These data indicate that the absorption of exosomes released from obesity adipose tissue including lower level of miR-141-3p than healthy adipose tissue into hepatocytes can significantly inhibit the insulin sensitivity and glucose uptake. Thus, our study may certify a novel mechanism that the secretion of “harmful” exosomes from obesity adipose tissues cause insulin resistance.
2020-01-27 | GSE109739 | GEO
Project description:Background Reduced endometrial receptivity is a major factor for impaired fertility in endometriosis (EMS). Endometrial deposition of collagen I proteins may account for poor endometrial receptivity in endometriosis. Methods We investigated the expression of collagen I expression in endometrium of endometriosis patients and in constructed EMS mice model. Effect of collagen I on ESCs was evaluated. Co-culture of exosomes with ESCs was conducted to evaluate the uptake of exosomes by different endometrial cell lines and the effect on decidualization of eutopic ESCs and embryo implantation. MiRNA expression profiles were compared between ectopic ESC derived exosomes and eutopic ESC derived exosomes. Luciferase reporter and its mutant plasmids were applied to confirm the direct target of miR-25-3p. Findings Here we found endometrial collagen I deposition with impaired decidualization in endometriosis patients and EMS mice model. Treatment of collagen I with ESCs contributed to impaired decidualization and inhibited BLS expansion in vitro. Endometriotic stromal cell-derived exosomes were detected in eutopic endometrium and the ectopic endometrial stromal cell derived exosomes were more taken-up by the same cell line in eutopic endometrium. Treatment of endometriotic stromal cell-derived exosomes increased the expression of endometrial collagen I in vitro and in vivo, while inhibited BLS expansion. Exosomal miR-25-3p was significantly increased in endometriotic stromal cell-derived exosomes compared with control group, and PTEN is a certain target of miR-25-3p. The promotion of endometrial miR-25-3p significantly increased collagen I expression in vitro through the PTEN/Akt pathway. Interpretation These results suggested that endometriotic stromal cell-derived exosomal miR-25-3p played key role in inducing endometrial collagen I deposition to impair embryo expansion in endometriosis via PTEN/Akt pathway. Funding National Nature Science Foundation of China (82271702), National Natural Science Foundation of China (81771537). Keywords: endometriosis; exosome; collagen I; miRNA; collagen deposition
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Project description:The salivary microbiota and its association with inflammatory mediators in periodontitis
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Project description:Profiling of plasma-derived exosomal RNA expression in patients with periodontitis: a pilot study
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Project description:The composition of the salivary microbiota has been reported to differentiate between patients with periodontitis, dental caries and orally healthy individuals. Thus, the purpose of the present investigation was to compare metaproteomic profiles of saliva in oral health and disease. Stimulated saliva samples were collected from 10 patients with periodontitis, 10 patients with dental caries and 10 orally healthy individuals. Samples were analyzed by means of shotgun proteomics. 4161 different proteins were recorded out of which 1946 and 2090 were of bacterial and human origin respectively. The human proteomic profile displayed significant overexpression of the complement system and inflammatory mediators in periodontitis and dental caries. Bacterial proteomic profiles and functional annotation were very similar in health and disease. Data revealed multiple potential salivary proteomic biomarkers of oral disease. In addition, comparable bacterial functional profiles were observed in periodontitis, dental caries and oral health, which suggest that the salivary microbiota predominantly thrives in a planktonic state expressing no characteristic disease-associated metabolic activity. Future large-scale longitudinal studies are warranted to reveal the full potential of proteomic analysis of saliva as a biomarker of oral health and disease.
2017-03-29 | MSV000080763 | MassIVE
Project description:Periodontitis is a chronic inflammatory disease resulting from a dysbiosis of the dental biofilm and a dysregulated host response in susceptible individuals. It is characterized by periodontal attachment destruction, bone resorption, and eventual tooth loss. Salivary biomarkers have been sought to predict and prevent periodontitis. This comparative study analyzed the salivary proteome of 30 individuals with chronic periodontitis (CP) and 10 with periodontal health (PH), and correlated specific proteins with clinical parameters of disease by using mass spectrometry. Stimulated whole saliva was obtained and pooled for 5 healthy controls and 15 CP patients, precipitated with TCA, digested enzymatically with trypsin and analyzed by an LTQ Orbitrap Velos equipped with a nanoelectrospray ion source. A wide range of salivary proteins of various functions was significantly reduced in CP individuals, whereas salivary acidic proline-rich phosphoprotein, submaxillary gland androgen-regulated protein, histatin, fatty acid-binding protein, thioredoxin, and cystatin were predominant in diseased patients and correlated significantly with signs of periodontal attachment loss and inflammation. Specific salivary proteins were associated with PH and CP. These differences in salivary proteome profiles may contribute to the identification of disease indicators or signatures and the improvement of periodontal diagnosis.
2020-05-20 | PXD015024 | Pride